Zusammenfassung

Host recognition is the crucial first step in
infectious disease pathogenesis. Recognition allows pathogenic
bacteria to identify suitable niches and deploy appropriate
phenotypes for successful colonization and immune
evasion. However, the mechanisms underlying host recognition
remain largely unknown. Mounting evidence suggests
that urocanate—an intermediate of the histidine degradation
pathway—accumulates in tissues, such as skin,
and acts as a molecule that promotes bacterial infection
via molecular interaction with the bacterial regulatory protein
HutC. In Gram-negative bacteria, HutC has long been
known as a transcriptional repressor of hut genes for the
utilization of histidine (and urocanate) as sources of carbon
and nitrogen. Recent work on the opportunistic human
pathogen Pseudomonas aeruginosa and zoonotic pathogen
Brucella abortus shows that urocanate, in conjunction with
HutC, plays a significant role in the global control of cellular
metabolism, cell motility, and expression of virulence
factors. We suggest that in addition to being a valuable
source of carbon and nitrogen, urocanate may be central to
the elicitation of bacterial pathogenesis.